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Research articleMolecular and Cellular Microbiology (MCM) | Biochemistry and Physiology
An Analog of the Antimicrobial Peptide CopA5 Inhibits Lipopolysaccharide-Induced Macrophage Activation
1Divison of Life Science and Chemistry, College of Natural Science, Daejin University, Pocheon 11159, Republic of Korea, 2Department of Agricultural Biology, National Academy of Agricultural Science, RDA, Wanju 55365, Republic of KoreaReceived: July 28, 2016; Accepted: October 11, 2016
J. Microbiol. Biotechnol. 2017; 27(2): 350-356
Published February 28, 2017
Copyright © The Korean Society for Microbiology and Biotechnology.
AbstractWe previously reported that the CopA3 peptide (LLCIALRKK, D-form) originally isolated from the Korean dung beetle has antimicrobial and immunosuppressive effects. However, the high cost of producing the synthetic peptide, especially the D-form, has limited the development of CopA3 for therapeutic purposes. Here, we investigated whether the CopA3 deletion derivative, CopA5, which is composed of only five amino acids (LLCIA) and has the L-form structure, could inhibit the lipopolysaccharide (LPS)-induced activation of macrophages. Peritoneal exudate macrophages (PEM) were isolated from mice and exposed to LPS in the presence or absence of CopA5, and biomarkers of macrophage activation were measured. Our results revealed that LPS-induced nitric oxide (NO) production, tumor necrosis factor (TNF)-α secretion, and phagocytic activity of PEM were significantly inhibited by CopA5 treatment. Similar to CopA3, the structurally modified CopA5 peptide had no cell toxicity (as assessed by measurement of cell viability loss and apoptosis) in PEM. Moreover, the LPS-induced upregulation of the activating phosphorylation of signal transducer and activator of transcription 1 (STAT1) was markedly inhibited by CopA5 treatment. These results suggest that, similar to CopA3, CopA5 inhibits macrophage activation by inhibiting STAT1 phosphorylation and blocking the release of NO and TNF-α. CopA5 may therefore prove therapeutically useful in the realm of immune suppression.
KeywordsAntimicrobial peptide, lipopolysaccharide, macrophages, immunosuppressive agent, signal transduction, STAT1